Signaling through the B-cell receptor (BCR) can lead to a range of biological outputs depending upon, in part, the developmental stage of the B-cell. Faulty signaling through the BCR can cause disregulation of the B-cell function and/or the formation of auto-antibodies which may lead to the auto-immune and/or inflammatory diseases. Therapeutics, such as Rituxan, which deplete B-cells are effective in the treatment of inflammatory diseases such as rheumatiod arthritis. Bruton's Tyrosine Kinase (BTK) is a member of the TEC family of kinases and is a regulator of B-cell development, activation, signaling and survival. BTK is downstream of the BCR. In humans, mutation of BTK causes X-linked agammaglobuliaemia results in a compromised immune system, impaired maturation of B-cells, decreased peripheral B-cell levels and reduced calcium mobilization following stimulation through the BCR. Further evidence for the role of BTK in autoimmune and inflammatory diseases has been established utilizing both BTK knock-out mouse models and pharmacological inhibitors. In addition to to B-cells, BTK is expressed on several other cell types that may contribute to disease, for example: mast cells, basophils, neutrophils, monocytes and osteoclasts. From this prespective it is clear that BTK inhibitors should provided substantial therapeutic benefit for patients afflicted with, for example: multiple sclerosis, type I diabetes, rheumatoid arthritis, SLE, idiopathic thrombocytopenic purpura, myasthenia gravis, allergic rhinitis, Sjögren's syndrome, B-cell lymphoma and leukemia.